Peptic ulcer Flashcards
1
Q
What is a peptic ulcer?
A
a mucosal break penetrating the muscularis mucosa
2
Q
What is an erosion?
A
a lesion superficial to the muscularis mucosa
3
Q
difference between peptic ulcer & erosion
A
peptic ulcer penetrates muscularis mucosa but erosion is superficial to it
4
Q
which one is more common, duodenal or gastric ulcer?
how many times more common?
A
dudeonal ulcer
5x
5
Q
lifetime risk of peptic ulcer
A
10%
6
Q
where is “duodenal bulb”?
A
the portion of the duodenum closest to the stomach (first 5cm of duodenum)
7
Q
over 95% of peptic ulcers are in ___ and ___
A
duodenal bulb and antrum
8
Q
peptic ulcer more in male of female?
A
slightly more in male
9
Q
common age of duodenal ulcers and gastric ulcers
A
DU: 30 - 55 yrs
GU: 55 - 75 yrs
10
Q
H. pylori is associated more with ___ ulcers
Aspirin and NSAIDs are associated more with ___ ulcers
A
H. pylori - duodenal
Aspirin and NSAIDs - gastric
11
Q
2 main factors in the pathophysiology of peptic ulcers:
A
H. pylori and NSAIDs
12
Q
helicobacter pylori microbiology
A
spiral-shaped, flagellated, Gram-negative bacillus with urease activity
13
Q
H. pylori is seen in __% of DUs and __% of GUs
A
DU - 90%
GU - 70%
14
Q
Urease changes ____ to ____ .
function:
A
Urease changes urea to ammonia
ammonia is alkaline, it helps resist acid
15
Q
how and when is H. pylori transmitted?
A
orally, mostly during childhood
16
Q
H. pylori is mostly in the ___
A
antrum
17
Q
If H. pylori is in the duodenum, it is associated with
A
metaplastic gastric epithelium
18
Q
Ulcer disease develops in __% of infected people
A
10%
19
Q
H pylori GU tends to occur at the junction of ___ and ___
A
body and antrum
20
Q
risk of GU and DU in long term NSAID use
A
GU: 10 - 20 %
DU: 2 - 5%
21
Q
There is greater risk of ulcer from NSAIDs in:
A
first 3 months of therapy >60 yrs Hx of ulcer NSAIDs + aspirin steroids anticoagulants co-morbidities
22
Q
Mucosal injury and, thus, peptic ulcer occur when the balance between the ____ factors and the ______ mechanisms is disrupted
A
aggressive defensive
23
Q
Aggressive factors (factors that cause ulcers)
A
NSAIDs h. pylori alcohol bile salts acid pepsin
24
Q
defensive mechanisms (protect against ulcers)
A
tight intercellular junctions mucus bicarbonate mucosal blood flow cellular restitution epithelial renewal
25
pathophysiolofy of H. pylori causing ulcers:
H pylori interact with G and D cells causing increased gastrin and hence acid production, mostly localized resulting in ulcer
26
In patients infected with H pylori, high levels of ___ and ____ and reduced levels of ____ have been measured
high: gastrin & pepsinogen
low: somatostatin
27
Virulence factors produced by H pylori:
urease
catalase
vacuolating cytotoxin
lipopolysaccharide
28
pathophysiology of H. Pylori causing duodenal ulcers:
increased gastric secretion + reduced duodenal bicarbonate secretion
= low pH
= gastric metaplasia
= duodenitis (predisposes to ulcers)
29
Non-selective NSAIDs inhibit __ synthesis
PG
30
Non-selective NSAIDs inhibit PG synthesis via _____ inhibition of ____
reversible
both cox1 and cox2
31
Aspirin causes _____ inhibition of __________
irreversible
cox1, cox2 and platelets aggregation
32
Coxibs are
selective cox2 inhibitors
33
the principal enzyme involved with cyto-protection in stomach and duodenum
Cox1
34
Coxibs reduce incidence of ___ by 75% compared with nsNSAIDs
ulcers
35
nsNSAIDS:
non-selective non-steroidal anti-inflammatory drugs
36
Coxibs reduce incidence of endoscopicallay visible ulcers by __% compared with nsNSAIDs
75
37
Coxibs result in __% reduction in incidence of serious complications of petic ulcers (obstruction, bleeding, perforation)
50%
38
risk of CVS complications (MI, CVA) with Coxib vs placebo
2 fold higher with coxibs
39
the only nsNSAIDs that do not increase risk of CV events:
Aspirin & naproxen
40
even low dose aspirin can increease risk of bleeding by:
2 fold
41
Risk factors for GIB
1. Hx of PU/GIB
2. Combining aspirin and NSAIDs or coxibs (10 fold increased PU complications than each alone)
3. H.pylori + low dose aspirin (3 fold increased complications)
42
Less than 5-10 % of ulcers are caused by other conditions:
```
Acid hypersecretion/ZES
Systemic mastocytosis
CMV/transplant patients
Crohn disease
Lymphoma
Medications/alendronates
Chronic medical illness (cirrhosis, CKD…)
Rarely idiopathic
```
43
clinical features of peptic ulcer
asymptomatic (20%, present with complications) (60% of NSAID ulcers)
epigastric pain (80 - 90 %) - not severe, dull, gnawing, aching, hunger-like
dyspepsia
44
Alarm features that warrant prompt gastroenterology referral include:
```
bleeding
anemia
early satiety
unexplained weight loss
progressive dysphagia or odynophagia
recurrent vomiting
FHx of GI cancer
```
45
Food aggravates or relieves pain?
stomach -
duodenum -
stomach - aggravates
| duodenum - relieves
46
50% of peptic ulcers are relieved with food,
| pain recurds in __ - __ hours
2 - 4 hours
47
_/3 of DUs and _/3 of GUs cause nocturnal pain that awakens the patient
2/3 of DUs 1/3 of GUs
48
nausea and anorexia may occur with GU/DU?
GU
49
is significant vomiting and weight loss normal for peptic ulcer?
no, it could be GOO or malignancy
50
physical examination can show what in peptic ulcers?
deep epigastric tenderness
51
lab investigation results in uncomplicated ulcers:
normal
52
Lab. tests may be ordered to look for complications or other diagnoses like:
Anemia (blood loss)
Leukocytosis (penetration / perforation)
Raised amylase in severe epigastric pain (pancreatic penetration / perforation )
53
what test do we do if we suspect ZES?
fasting gastrin level
54
test of choice for peptic ulcers:
endoscopy
55
risk of malignancy is DU
0
56
when do u biopsy a gastric ulcer?
always
57
if ulcer doesnt heal after how long will u be suspicious its malignant?
3 months
58
CT for peptic ulcer can show what?
perforation
obstruction
penetration
59
CLO stands for _________ and is also known as __________
Campylobacter-like organism
| Rapid Urease Test
60
explain how the CLO test is done:
A biopsy of mucosa is taken from the antrum of the stomach, and is placed into a medium containing urea and an indicator such as phenol red.
The urease produced by H. pylori hydrolyzes urea to ammonia, which raises the pH of the medium, and changes the color of the specimen from yellow (NEGATIVE) to red (POSITIVE)
61
during what is the CLO test done?
gastroscopy
62
H pylori tests
```
CLO test
histology
urea breath test
stool antigen
serum antibody
```
63
what do u need to do before Urea breath and stool antigen test?
Stop PPI for 1-2 weeks and antibiotic for 2-4 weeks before
64
DDx of peptic ulcer
```
Dyspepsia
Atypical GERD
Biliary disease
Chronic pancreatitis
Abdominal malignancy/gastric, pancreatic in particular
Carbohydrate malabsorption
Chronic mesenteric ischemia
```
65
DDx for acute severe pain (instead of perforated/penetrated PU)
```
Acute pancreatitis
Acute cholecystitis
Choledaucholithiasis
Esophageal rupture
Gastric volvulus
Ruptured aortic aneurysm
```
66
Treatment for PU involves doing what?
acid suppression
h pylori eradication
removing nsaid
67
what do PPIs do?
permenantly inhibit proton pump
68
after PPI, restoration of acid require new pump with half life of __ hours
18
69
PPIs have a half life of __ hours
60 min
| 24 hrs
70
24 hr acid secretion inhibition
PPI: %
H2R antagonists: %
PPI >90%
| H2R antagonists <65%
71
with PPI, >90% of PUs heal within
GU:
DU:
GU: 8 weeks
DU: 4 weeks
72
when in the day are PPIs taken?
30 min before breakfast / long fasting
73
In 3% of patients on long term PPI ____ level increase considerably but normalizes in 2 weeks after stopping
gastrin
74
which ones better. H2R antagonists or PPIs?
PPIs
75
All H2R antagonists can inhibit nocturnal acid but not _____ acid
post prandial
76
when in the day are H2R antagonists given?
once at bedtime
they suppress nocturnal acid, not post prandial like PPIs so not given before meals
77
with H2R antagonists,85 - 90% of PUs heal within
GU:
DU:
GU: 8 weeks
DU: 6 weeks
78
Agents enhancing mucosal defenses:
Bismuth
misoprostol
antacids
79
general regimen for H pylori eradication is ___ + ___
PPI + antibiotics (1 or more)
80
how does misoprostol work? (in the context of PUs)
Misoprostol is a synthetic prostaglandin E1 analog that stimulates prostaglandin E1 receptors on parietal cells in the stomach to reduce gastric acid secretion
81
duration of H pylori eradicatio is
1 - 2 weeks
82
Confirm h pylori eradication _ weeks after stopping antibiotics and _ weeks after stopping PPI
4
| 2
83
UBT:
urea breath test
84
explain the UBT
- urea capsule is swallowed
- h pylori urease breaks down the later to produce ammonia and CO2
- CO2 is detected in breath
85
re infection rate of h. pylori after eradication:
1 - 2 % per year
86
when an ulcer recurs, we should exclude
NSAIDs and hypoer-secretory states
87
if patient has ulcer but u cant stop NSAIDs
concomitant PPI once daily results in ulcer healing in __% in _ weeks
80% 8
88
All NSAID-associated ulcers should be tested for
H pylori
89
how to reduce NSAID induced ulcers
```
1- outweigh benefit against risks
2- lowest effective dose
3- shortest period
4- less irritant agent
5- avoid combination with steroids and anticoagulants unless necessary
```
90
All patients who require aspirin and anticoagulants should be given a
PPI
91
what percentage of ulcers don't heal by 8 weeks of 1 PPI / day?
2 PPI / day?
< 5%
almost all heal with 2
92
most common cause of refractory ulcers:
non compliance
93
causes of refractory ulcers
```
noncompliance
NSAIDs, aspirin, iron, biphosphonates
H pylori
ZES
malignancy (adenocarcinoma or lymphoma)
Crohn
infection (CMV, HSV, mucormycosis, TB, syphilis, candida)
ischemia
```
94
50% of UGIB are cuz of
peptic ulcers
95
UGIB from PU is significant in __%
10
96
what percent of PU bleeding stops spontaneously?
80%
97
mortality rate of bleeding PU
7%
98
mortality from bleeding PU is higher in:
```
elderly
comorbidities
hospital associated
persistent HPO
bright red blood in vomit / NGT
severe coagulopathy
```
99
H2RA for bleeding peptic ulcer
useless
100
Recurrent PU bleeding occur in _/3 within _ years if no specific treatment is given
1/3 in 3 yrs
101
if there is recurrent bleeding from PU and everything else failed, we do
surgical treatment endoscopically (<5%)
102
surgical mortality for bleeding PU is 6% but higher if:
>60 years
Comorbidities
Renal failure
Requiring >10 pints of blood
103
alternative surgical treatment to endoscopy in bleeding PU is
angiographic embolization
104
perforated peptic ulcer is usually in the
anterior wall of stomach and duodenum
105
in perforated PU, sudden severe abdominal pain that may generalize due to
chemical peritonitis
106
what patients have no symptoms of perforated PU and present late with complications (bacterial peritonitis, sepsis and shock)
elderly
| steroids
107
signs of perforated PU
rigid & quiet abdomen
| rebound tenderness
108
HPO can occur when bacterial peritonitis develops therefore when HPO is present at the start think of:
Ruptured aortic aneurysm
Pancreatitis
Mesenteric ischemia
109
lab signs of perforated PU
leukocytosis and increased serum amylase
110
why does serum amylase increase in perforated PU?
Amylase leaks through perforation and get absorbed
111
diagnosis of perforated PU is by
CT
112
absence of free air in perforated PU leads to misdiagnosis of
pancreatitis / cholecystitic / appendicitis
113
treatment of perforated PU is
surgery
114
GOO occurs in
2
115
GOO is caused by
edema or fibrosis of pylorus or bulb
116
GOO is less from PU cuz we treat PUs better, now its mostly cuz of
gastric neoplasm and duodenal obstruction by extrinsic compression
117
clinical features of GOO
early satiety
vomiting
weight loss (1 to several hours after eating, contains partially digested food)
118
blood tests in GOO shows
Hypokalemia and alkalosis
119
examination of patient with GOO shows
succussion splash
120
management of GOO
```
admission
IV fluid / saline and KCL
IV PPI
NG decompression
endoscopy after 1 - 3 days to diagnose
```
```
if benign:
pneumatic balloon dilatation or surgery
vagotomy and antrectomy
vagotomy and pyloroplasty
truncal vagotomy
gastrojejunostomy
```
